Jia Ming Nickolas Teo, Weixin Chen, Guang Sheng Ling
{"title":"Neutrophil plasticity in liver diseases.","authors":"Jia Ming Nickolas Teo, Weixin Chen, Guang Sheng Ling","doi":"10.1093/jleuko/qiae222","DOIUrl":null,"url":null,"abstract":"<p><p>The liver has critical digestive, metabolic, and immunosurveillance roles, which get disrupted during liver diseases such as viral hepatitis, fatty liver disease, and hepatocellular carcinoma. While previous research on the pathological development of these diseases has focused on liver-resident immune populations, such as Kupffer cells, infiltrating immune cells responding to pathogens and disease also play crucial roles. Neutrophils are one such key population contributing to hepatic inflammation and disease progression. Belonging to the initial waves of immune response to threats, neutrophils suppress bacterial and viral spread during acute infections, and have homeostasis-restoring functions. Whereas during chronic insults, they display their plastic nature by responding to the inflammatory environment and develop new phenotypes alongside longer lifespans. This review summarizes the diversity in neutrophil function and subpopulations present at steady state, during liver disease, and during liver cancer.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6000,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Leukocyte Biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/jleuko/qiae222","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
The liver has critical digestive, metabolic, and immunosurveillance roles, which get disrupted during liver diseases such as viral hepatitis, fatty liver disease, and hepatocellular carcinoma. While previous research on the pathological development of these diseases has focused on liver-resident immune populations, such as Kupffer cells, infiltrating immune cells responding to pathogens and disease also play crucial roles. Neutrophils are one such key population contributing to hepatic inflammation and disease progression. Belonging to the initial waves of immune response to threats, neutrophils suppress bacterial and viral spread during acute infections, and have homeostasis-restoring functions. Whereas during chronic insults, they display their plastic nature by responding to the inflammatory environment and develop new phenotypes alongside longer lifespans. This review summarizes the diversity in neutrophil function and subpopulations present at steady state, during liver disease, and during liver cancer.
期刊介绍:
JLB is a peer-reviewed, academic journal published by the Society for Leukocyte Biology for its members and the community of immunobiologists. The journal publishes papers devoted to the exploration of the cellular and molecular biology of granulocytes, mononuclear phagocytes, lymphocytes, NK cells, and other cells involved in host physiology and defense/resistance against disease. Since all cells in the body can directly or indirectly contribute to the maintenance of the integrity of the organism and restoration of homeostasis through repair, JLB also considers articles involving epithelial, endothelial, fibroblastic, neural, and other somatic cell types participating in host defense. Studies covering pathophysiology, cell development, differentiation and trafficking; fundamental, translational and clinical immunology, inflammation, extracellular mediators and effector molecules; receptors, signal transduction and genes are considered relevant. Research articles and reviews that provide a novel understanding in any of these fields are given priority as well as technical advances related to leukocyte research methods.